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Chapter 24 MENINGITIS168

WEBSITE

Infectious Diseases Society of America: www.idsociety.org.

BIBLIOGRAPHY

1. Attia J, Hatala R, Cook DJ, et al: Does this adult patient have acute meningitis? JAMA 282:175–181, 1999.

2. Chaudhuri A: Adjunctive dexamethasone treatment in acute bacterial meningitis. Lancet Neurol 3:54–62, 2004.

3. Edlow JA: Headache. In Wolfson AB, editor: Hardwood-Nuss’ clinical practice of emergency medicine, ed 4,

Philadelphia, 2005, Lippincott Williams & Wilkins, pp 94-100.

4. Euerle B: Spinal puncture and cerebrospinal ﬂuid examination. In Roberts JR, Hedges JR editors: Clinical

procedures in emergency medicine, ed 4, Saunders, 2004, pp 1197–1222.

5. Quagliarello VJ, Scheld WM: Treatment of bacterial meningitis. N Engl J Med 336:708–716, 1997.

6. Sadoun T, Singh A: Adult acute bacterial meningitis in the United States: 2009. update. Emergency Medicine

Practice 11(9): 1–25, 2009.

7. Talan DA: New concepts in antimicrobial therapy for emergency department infections. Ann Emerg Med

34:503–516, 1999.

8. Ziai WC, Lewin III JJ: Update in the diagnosis and management of central nervous system infections.

Neurologic Clinics 26: 427–468, 2008.

169

V. RESPIRATORY SYSTEM

CHAPTER 25

BREATHING AND VENTILATION

John L. Kendall, MD, and Ryan Paterson, MD

1. How useful is the respiratory rate in the evaluation of a patient?

The respiratory rate is invaluable as a vital sign. Normal respiratory rate in children varies

with age, whereas adults typically breathe 12 to 16 times per minute. As a testament to its

usefulness, the respiratory rate can be helpful in the diagnosis of many conditions other

than those with primary pulmonary pathology. For example, it is elevated in patients with

anemia, arteriovenous ﬁstula, pregnancy, cyanotic heart disease, metabolic acidosis, febrile

illness, central nervous system pathology, anxiety, and those at high altitude. It is important

that the respiratory rate be counted carefully for at least 30 seconds. The respiratory rate is

often incorrectly estimated from a short period of observation.

2. Which breathing patterns are associated with pathologic conditions?

Kussmaul respirations are deep, rapid breaths that are associated with metabolic

acidosis.

Cheyne-Stokes breathing comprises respirations that wax and wane cyclically so that

periods of deep breathing alternate with periods of apnea. Causes include congestive

heart failure (CHF), hypertensive crisis, hyponatremia, high altitude illness, and head

injury.

Ataxic breathing is characterized by unpredictable irregularity. Breaths may be

shallow or deep and may stop for short periods. Causes include respiratory

depression and brain stem injury at the level of the medulla.

3. Which pulmonary function tests are commonly used in the ED?

Other than the respiratory rate, the most useful pulmonary function test for ED patients

is the peak expiratory ﬂow rate. It is measured by having a patient exhale at a maximum

rate through a peak ﬂowmeter. Normal values range from 350 to 600 L/min in adults.

Lower levels are characteristic of increased airway resistance as commonly seen in

asthma and chronic obstructive pulmonary disease (COPD) exacerbations. Patients who

present with values of less than 100 L/min have severe airﬂow obstruction. Comparing a

patient’s current peak expiratory ﬂow rate to his or her personal best can provide good

insight into the severity of respiratory distress and necessary treatment. Serial

measurements are helpful for objectively quantifying response to treatment. A less

commonly used test is the forced end-expiratory volume at 1 second, which helps

quantify the severity of obstructive and restrictive lung disease.

4. How does pulse oximetry work?

Pulse oximetry is based on a combination of spectrophotometry and plethysmography.

Spectrophotometry is based on the Beer-Lambert law, which holds that optical

absorbance is proportional to the concentration of a substance and the thickness of the

medium. Using this principle, the absorbance of light within a pulsatile vascular bed is

used to distinguish between oxyhemoglobin (O

Hb) and reduced hemoglobin (Hb).

Plethysmography measures the tissue displacement caused by an arterial pulse. This

allows for assessment of the increase in light absorption caused by local arterial ﬂow

compared with the background of composite tissues and venous blood.

Plethysmography also allows determination of the heart rate.

Chapter 25 BREATHING AND VENTILATION170

Pulse oximeters function by placing a pulsatile vascular bed between a light-emitting diode

(LED) and a detector. Light is transmitted through the tissue at two wavelengths, 660 nm

(primarily absorbed by O

Hb) and 940 nm (primarily absorbed by Hb), allowing differentiation

of O

Hb from Hb. The detector compares the concentration of O

Hb and Hb and displays the

result as a percent saturation.

5. How can pulse oximetry be useful? In which situations can it yield false

readings?

Pulse oximetry is useful when monitoring arterial O

Hb saturation in cardiopulmonary

disorders; monitoring oxygen saturation during conscious sedation, airway management, or in

patients with a decreased level of consciousness; or quantifying the arterial O

Hb saturation

response to therapeutic interventions. Situations in which the usefulness of pulse oximetry is

limited include vasoconstriction, excessive movement, low O

Hb saturations (,83%),

intravascular dyes, exposure of the measuring sensor to ambient light sources, and when nail

polish is present. Oxygen saturation measurements may be falsely elevated in the presence of

carboxyhemoglobin and falsely decreased in the presence of methemoglobin.

KEY POINTS: PULSE OXIMETRY

1. Pulse oximetry measures oxygenation, not ventilation.

2. Poor peripheral perfusion is a frequent reason pulse oximeters provide unreliable readings.

6. Why can a good pulse oximetry reading be falsely reassuring?

Clinicians often rely on the pulse oximeter as part of monitoring a patient’s respiratory status,

particularly when using procedural sedation. The pulse oximeter only measures oxygenation

and provides no information regarding CO

exchange and thus does not assess for adequate

ventilation. A preoxygenated patient can be apneic for several minutes without an appreciable

decrease in oxygen saturation, while signiﬁcant hypercarbia is developing. Although the pulse

oximeter has become indispensable, the clinician must always remember that it only assesses

one part of a patient’s respiratory status.

7. What is end-tidal CO

(EtCO

) and when is its monitoring useful?

EtCO

is another monitoring device used to evaluate ventilation, and when combined with the

pulse oximeter, it provides a more complete evaluation of the patient’s respiratory status.

EtCO

monitors exhaled CO

displaying its concentration in both numerical and graphical

format. The CO

concentration in the breath correlates directly with the concentration of CO

in the alveoli. The CO

in the alveoli is dependent on the ventilation/perfusion (V/Q)

relationship, which is inﬂuenced by a number of physiologic and pathologic states. A CO

increase or decrease may represent the earliest change in a patient’s ventilation and perfusion

states. EtCO

is currently being used in a number of ways:

During conscious sedation

In patients with sepsis to monitor perfusion status

During cardiopulmonary resuscitation (CPR) to monitor effectiveness of compressions

For monitoring airway response to treatment in patients with COPD and asthma

To monitor for tube placement or dislodgement by emergency medical services (EMS)

during intubation and transport

8. What percentage of fraction of inspired oxygen (FiO

) corresponds with the

various types of oxygen delivery systems?

The three primary means of oxygen delivery are nasal cannula, simple facemask, and

facemask with an oxygen reservoir. A nasal cannula can be used to deliver oxygen at rates of

Chapter 25 BREATHING AND VENTILATION 171

1 to 6 L/min. With a nasal cannula, every 1 L/min of ﬂow increase causes the FiO

to rise by

4%. As a result, a nasal cannula can deliver a FiO

between 25% and 45%. A simple facemask

relies on an oxygen ﬂow of 5 to 10 L/min with a resulting FiO

ranging from 35% to 50%.

A facemask with an oxygen reservoir has a constant ﬂow of oxygen so that higher

concentrations of oxygen can be achieved. A properly ﬁtted facemask with an oxygen

reservoir with a 15 L/min ﬂow rate can deliver up to 85% FiO

9. What is noninvasive ventilation?

It is a means of delivering positive-pressure ventilation without placing a nasotracheal or

endotracheal tube. As such, ventilatory assistance is possible without the risks of intubation

and mechanical ventilation. Careful selection of patients can make noninvasive ventilation a

useful tool to the emergency physician. Any patient who does not have an appropriate mental

status, is unable to protect the airway, or is unable to develop an adequate respiratory rate

would not be a good candidate for noninvasive ventilation.

10. What forms of noninvasive ventilation are available to emergency physicians?

The two most useful forms are mask continuous positive airway pressure (CPAP) ventilation

and bilevel positive airway pressure (BiPAP). Each method involves placing a tight-ﬁtting mask

over the patient’s face and delivering breaths by positive pressure.

CPAP delivers a continuous amount of positive airway pressure during and after inspiration

and expiration.

BiPAP not only provides a set positive pressure during exhalation but also delivers a set

inspiratory pressure when the patient initiates a breath. The inspiratory pressure is always

set higher than the expiratory pressure, can be sustained for various periods, and stops

when the patient ceases to inhale or begins to exhale.

11. In what circumstances would noninvasive ventilation be preferred over

standard invasive ventilation?

Noninvasive ventilation has been shown to be useful in many conditions, including pulmonary

edema, pneumonia, asthma, COPD, and nocturnal hypoventilation. In properly selected

patients, CPAP is particularly useful in the treatment of pulmonary edema and BiPAP in

respiratory distress due to COPD. Patients with COPD are notoriously difﬁcult to wean from

mechanical ventilators, and noninvasive ventilation can frequently be used to turn around

COPD patients in moderate respiratory distress who would otherwise have required standard

invasive ventilation. Lastly, some patients with advance directives forbidding mechanical

ventilation can beneﬁt from the respiratory support provided by noninvasive ventilation.

12. How do I determine the initial ventilator settings in someone who has just

been intubated?

Ventilator settings must take into account the patient’s oxygenation status and his or her

ventilation or acid-base status. The primary method for affecting the oxygenation of a patient

is to alter the FiO

and positive end-expiratory pressure (PEEP). Initially, intubated patients

should be given 100% oxygen or an FiO

of 1.00. Subsequently, if arterial blood gas analysis

reveals that the PaO

is high, the FiO

and PEEP may be lowered incrementally.

The main factors determining a patient’s ventilatory status are tidal volume and respiratory

rate. Changes in each are reﬂected by the CO

from arterial blood gas analysis. High

respiratory rates and large tidal volumes decrease the carbon dioxide level, whereas the

converse elevates the carbon dioxide level. Initially, the tidal volume can be estimated to be

8 to 10 mL/kg; for a 70-kg patient, that is 560 to 700 mL.

The initial respiratory rate varies depending on the clinical situation. On average, the rate

should be set between 10 and 16 breaths per minute.

13. Are ventilator settings always the same?

No. When you intubate a patient you must remember that you have now placed a bet that you

can do a better job directing that patient’s ventilation than his or her brain. Keep in mind that

Chapter 25 BREATHING AND VENTILATION172

your patient’s respiratory center has millions of years of evolution backing it up compared

with your measly few years of experience. Imagining how your patient’s respiratory center

would respond to the clinical situation and where the failure has occurred will help you to

determine the best ventilator settings for your patient. For example, a patient with an

obstructive condition such as asthma does best with small tidal volumes, high respiratory

rates, and low levels of PEEP. In contrast, a patient with a COPD exacerbation requires lower

respiratory rates, higher tidal volumes, no PEEP, and a prolonged expiratory time. Following

EtCO

and pulse oximetry can provide real-time feedback of the adequacy of your settings.

Other common ventilator settings for patients with closed head injury, CHF, metabolic

acidosis, and sepsis are shown in Table 25-1.

14. What are the different ventilator modes?

The main modes of ventilation are controlled mechanical ventilation (CMV), assist control

(AC), intermittent mandatory ventilation (IMV), and synchronized intermittent mandatory

ventilation (SIMV). In the CMV mode, the ventilator delivers a certain volume or pressure at a

preset rate, regardless of any ventilatory effort by the patient. AC is similar to CMV in that the

tidal volume or inspiratory pressure and minimum respiratory rate are set. It differs from CMV

by allowing patients to trigger the ventilator over a set minimum respiratory rate. IMV allows

the patient to breathe spontaneously without having a preset tidal volume or pressure. A set

rate similar to the CMV mode is in place. This allows the patient to breathe spontaneously,

while ensuring a set respiratory rate and tidal volume. SIMV differs from IMV in that the

ventilator senses the patient’s spontaneous respirations and does not deliver a breath if the

patient has already triggered the ventilator. This prevents stacking of respirations, which can

be a component of the IMV mode.

15. What is PEEP?

PEEP is pressure applied during expiration. PEEP prevents collapse of alveoli at end-expiration

leading to an increase in functional residual capacity. The end result is improved V/Q matching

in the pulmonary circulation, improving oxygenation. On the ﬂip-side, PEEP can induce

barotrauma, diminish venous return to the heart, and elevate intracranial pressure. PEEP is

usually set at 2.5 or 5.0 cm H

CHF, congestive heart failure; COPD, chronic obstructive pulmonary disease; FiO

, fraction of inspired oxygen;

PEEP, positive end-expiratory pressure.

American Heart Association: Pediatric Advanced Life Support Provider Manual, Dallas, 2002, American Heart

Association, p 109.

Condition

Tidal Volume

(mL/kg)

Respiratory Rate

(breaths per minute) FiO

PEEP

(cm H

Asthma 5–10 10–16 100% 2.5–10

COPD 8–12 6–8 100% None

Head injury 12–15 14–20 100% None

CHF 8–12 8–12 100% 5–10

Metabolic acidosis 8–12 14–20 100% 2.5–5

Sepsis 6 10–16 100% 2.5–5

TABLE 25-1. VENTILATOR SETTINGS ACCORDING TO CONDITION

Chapter 25 BREATHING AND VENTILATION 173

16. What is auto-PEEP?

Auto-PEEP develops when a positive-pressure breath is delivered before complete exhalation

of the previous breath. As a result, air becomes trapped and pressure within the lungs

increases. This leads to increased airway pressures, diminished venous return to the right

heart, and consequently hypotension. The increased airway pressures can lead to barotrauma,

pneumothorax, and inaccurate pulmonary artery catheter measurements. Auto-PEEP can be a

particular problem in the mechanical ventilation of COPD and asthmatic patients. The

immediate solution is to disconnect the ventilator circuit and allow a full exhalation followed

by appropriate changes to the ventilator settings.

17. What are the most common complications of mechanical ventilation?

The most common direct complication seen in the ED is barotrauma. High pressure can lead

to rupture of the alveolar wall, which can lead to pneumomediastinum, pneumothorax, tension

pneumothorax, pneumoperitoneum, and subcutaneous emphysema. Pneumonia leads the list

of ventilator complications overall, followed by sinusitis, tracheal necrosis, local trauma to the

nares and mouth, increased intracranial pressure, renal failure, hyponatremia, and ﬂuid

retention.

18. How do I approach a patient on a ventilator with acutely worsening

oxygenation or ventilation?

A systematic approach to this situation will serve you well. The DOPE mnemonic taught in

pediatric life support can be helpful in remembering the approach:

First remove the patient from the ventilator and have an assistant hand ventilate the patient.

Many problems involving a $30,000 ventilator can be solved with a $15 resuscitation bag.

Displacement: Conﬁrm the endotracheal tube is in the proper place by using some

combination of auscultation, CO

exchange, radiography, and direct visualization.

Obstruction: Conﬁrm that the endotracheal tube is patent by passing suction catheter.

Sometimes an endotracheal tube can become kinked simply due to patient positioning.

Pneumothorax: Conﬁrm that there is no evidence of barotrauma, usually by a combination

of physical examination and a chest radiograph.

Equipment: Conﬁrm that the ventilator circuit and ventilator itself are functioning properly.

KEY POINTS: VENTILATOR MANAGEMENT

1. Each clinical situation calls for a different approach to ventilator management.

2. Tidal volume and respiratory rate affect the patient’s ventilation and pCO

3. FiO

and PEEP affect the patient’s oxygenation and pO

4. Oxygenation and ventilation problems in patients on mechanical ventilators can be managed

by removing them from the ventilator and following the DOPE mnemonic.

174

CHAPTER 26

ASTHMA, CHRONIC OBSTRUCTIVE

PULMONARY DISEASE, AND PNEUMONIA

Rita K. Cydulka, MD, MS, and Scott Felten, MD, FACEP

ASTHMA

1. What is asthma and what are the presenting symptoms of asthma

exacerbation?

Asthma is a chronic inﬂammatory disorder of the airways, resulting in recurrent

episodes of wheezing, breathlessness, chest tightness, and coughing. The airway

inﬂammation contributes to airway hyperreactivity, airﬂow obstruction, and chronic

disease.

2. In addition to asthma, what should be included in the differential

diagnosis of wheezing?

Chronic obstructive pulmonary disease (COPD), congestive heart failure (CHF), foreign

body aspiration, anaphylaxis, epiglottitis, tracheobronchitis, reactive airway disease, viral

respiratory infections, and vocal cord dysfunction.

3. Which aspects of the asthmatic’s history are important to the current

exacerbation?

Ask questions regarding exposure to common precipitants, such as viral upper

respiratory tract infections, allergens, cold, exercise, and possible aspirin or

nonsteroidal anti-inﬂammatory drug use. Also important are duration and severity of

symptoms, past history and frequency of sudden exacerbations, prior hospitalizations

and intubations, number of recent ED visits, current medications, worsening of

symptoms while on or if weaning off corticosteroids, and other comorbidities.

Non-Caucasian race and lower socioeconomic standing are also risk factors for severity

requiring hospitalization.

4. Are there any helpful ancillary diagnostic tests?

Bedside spirometry provides a rapid, objective assessment of patients and serves as a

guide to the effectiveness of therapy. The forced expiratory volume in 1 second (FEV

)

and the peak expiratory ﬂow rate (PEFR) directly measure the degree of large airway

obstruction.

FEV

or PEFR >70% of predicted (or personal best) indicates mild obstruction

FEV

or PEFR 40%–69% of predicted (or personal best) indicates moderate

obstruction

FEV

or PEFR ,40% of predicted (or personal best) indicates severe obstruction

Pulse oximetry is a useful and convenient method for assessing oxygenation and

monitoring oxygen saturation during treatment. Most other tests, including arterial blood

gases, complete blood counts, and electrocardiograms, are not useful in the

management of asthma except in cases of active or impending respiratory failure. Chest

X-ray may be helpful if the patient does not respond to initial treatment or if a pulmonary

complication, such as foreign body obstruction, pneumonia, pneumomediastinum,

pneumothorax, or CHF, is suspected.

Chapter 26 ASTHMA, CHRONIC OBSTRUCTIVE PULMONARY DISEASE, AND PNEUMONIA 175

5. What are the key objectives when treating an asthma exacerbation? How are

they achieved?

The key objectives include correction of signiﬁcant hypoxemia, rapid reversal of airﬂow

obstruction, and reduction of the likelihood of recurrence of severe airﬂow obstruction.

First-line treatment includes b

-agonists and corticosteroids in moderate exacerbations,

and oxygen if needed. Ipratropium should be added when treating severe exacerbations. Relief

of airﬂow obstruction (bronchoconstriction) is usually accomplished by administration of

either intermittent or continuous doses of aerosolized b

-agonists. Studies contain mixed

conclusions as to whether there is any added clinical beneﬁt to levalbuterol in comparison to

racemic formulations. Current evidence does not suggest an improved beneﬁt from

intravenous b

-agonists compared to aerosol. Early administration of systemic corticosteroids

addresses the inﬂammatory component of acute asthma and has been demonstrated to

prevent some hospitalization, although beneﬁcial effects of corticosteroids are often not noted

until several hours after administration. High-dose inhaled corticosteroids may have some

beneﬁt in the acute setting and can be continued safely by patients already on inhaled

steroids. Aerosolized ipratropium should be added if FEV

or PEFR is ,40% of predicted

because studies reveal that they increase pulmonary function modestly and decrease need for

hospitalization in these patients. Hypoxemia is usually corrected by administration of

supplemental oxygen with a goal of oxygen saturation of 90% to 95%. (See Table 26-1.)

Epinephrine or terbutaline may be administered subcutaneously to patients unable to

coordinate aerosolized treatments. Theophylline is not recommended in the acute setting.

6. How can I determine if my patients are improving?

Ask them how they feel, re-examine them, and obtain objective measures of pulmonary

function. Either FEV

or PEFR (the best of three attempts) should be obtained on presentation

and after treatment and compared with the patient’s percent predicted (or personal best) FEV

or PEFR, if known, to determine the need for more aggressive therapy or hospitalization.

7. What measures are available if my patient isn’t responding as expected?

Magnesium, heliox, ketamine, and continuous positive-pressure ventilation may offer some

beneﬁts when all other treatment modalities have failed and patients remain in severe status

after conventional therapy. Magnesium sulfate has been noted to help reverse bronchospasm

in conjunction with standard therapy if PEFR is 25% or less of predicted but is not useful in

patients with mild or moderate obstruction. Although widely discussed in the literature, the

data for ketamine, heliox, and continuous positive-pressure ventilation are less compelling.

There are no absolute indications for intubation except for respiratory arrest and coma.

Possible indication for intubation includes exhaustion, worsening respiratory distress,

persistent or increasing hypercarbia, and changes in mental status. Intubate semielectively,

before the crisis of respiratory arrest, because intubation is difﬁcult in patients, who have

asthma.

8. How should I decide whether a patient can be discharged or requires

hospitalization?

Disposition of patients is usually determined by clinical response after three doses of

aerosolized b

-agonist therapy; ipratropium (if used); and corticosteroids. If patients have

clear breath sounds, are no longer dyspneic or are back to baseline, and have an FEV

PEFR 70% of predicted, they may be discharged home. Patients with an incomplete response

to treatment, that is, FEV

between 50% and 70% of predicted and mild dyspnea, can be

considered for discharge after assessing their individual circumstances. Patients with a poor

response to bronchodilators, that is, FEV

,50% of predicted and who have moderate to

severe symptoms after treatment, require hospitalization. If an ED observation capability

exists, observation for 4 to 6 hours poststeroid administration will decrease the number of

inpatient admissions.

Chapter 26 ASTHMA, CHRONIC OBSTRUCTIVE PULMONARY DISEASE, AND PNEUMONIA176

9. What should be considered at time of discharge?

Patients who received corticosteroids acutely should continue oral steroid therapy at home for

3 to 10 days. For courses of less than 1 week, there is no taper required. For a 10-day course,

there remains no need to taper if the patients are concurrently taking inhaled formulations.

Dosing parameters are controversial, so choose a moderate regimen (about 40–50 mg

prednisone per day); Patients not already on controller medications who have mild persistent

asthma should be started on low-dose inhaled corticosteroids or oral leukotriene modiﬁers, such

as zaﬁrlukast or montelukast. Long-acting b-agonists, such as salmeterol, should be added to

the regimen of patients with moderate persistent asthma who are inadequately controlled on

inhaled corticosteroids. All patients should be advised to use their short-acting b-agonists on a

regularly scheduled basis for a few days and then as needed. Patient education should be

provided at discharge, as well as an appointment for a follow-up visit within several weeks.

10. Does pregnancy change the management of acute asthma?

No. It is important to treat pregnant asthmatics aggressively to prevent maternal hypoxia and

subsequent fetal morbidity and mortality. Patients should not be undertreated because of fear

of teratogenicity; the risks from respiratory failure and severe acute asthma are greater than

from therapy with standard medications. The standard therapy and dosages are the same.

COPD, chronic obstructive pulmonary disease.

*Exercise extreme caution in patients with known coronary artery disease.

Medications Dosage and Route

Inhaled short-acting b

–agonists

Albuterol Nebulizer solution (5 mg/mL) 2.5–5 mg every 20 minutes for three doses,

then 2.5–10 mg every 1–4 hours as needed,

or 10–15 mg/hour continuously or

7.5 mg bolus

MDI (90 mg/puff): must be used with

spacer device

Four to eight puffs every 20 minutes up to

4 hours, then every 1–4 hours as needed

Systemic (injected) b

-agonists*

Epinephrine 1:1000 (1 mg/mL) 0.3–0.5 mg every 20 minutes for three

doses subcutaneously

Terbutaline (1 mg/mL) 0.25 mg every 20 minutes for three doses

subcutaneously

Inhaled anticholinergics

Ipratropium bromide nebulizer solution

(0.25 mg/mL)

0.5 mg every 30 minutes for three doses

then every 2–4 hours as needed

MDI (18 mg/puff): must be used with

spacer device

Four to eight puffs as needed

Systemic corticosteroids

Prednisone or prednisolone

Methylprednisolone

40–60 mg by mouth

125 mg intravenously

TABLE 26-1. MEDICATIONS USED TO TREAT ASTHMA AND COPD EXACERBATIONS

Chapter 26 ASTHMA, CHRONIC OBSTRUCTIVE PULMONARY DISEASE, AND PNEUMONIA 177

KEY POINTS: EMERGENCY TREATMENT OF ASTHMA

1. Relieve signiﬁcant hypoxemia: oxygen.

2. Reverse airﬂow obstruction: b-agonists 1 ipratropium.

3. Reduce the likelihood of recurrence: corticosteroids.

4. Provide objective measure of improvement: PEFR or FEV1.

5. Adequate discharge planning includes education, medications, and follow-up.

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

11. What is COPD and what are the presenting symptoms of a COPD exacerbation?

COPD is a disease characterized by chronic airﬂow limitation that is not fully reversible, is

progressive, and is associated with an abnormal inﬂammatory response to noxious particles

or gases. It is a combination of small airway disease and parenchymal destruction. It includes

emphysema and chronic bronchitis and can coexist with asthma. The characteristic symptoms

of COPD are cough, sputum production, and dyspnea on exertion. Exacerbations are

characterized by increased dyspnea, often accompanied by wheezing and chest tightness,

increased cough and sputum, change in color or thickness of sputum, and fever. Smoking,

exposure to occupational dusts and chemicals, and air pollution are the most common causes

of COPD.

12. In addition to COPD, what should be included in the differential diagnosis?

In patients who present with wheezing, the differential diagnosis includes asthma, CHF,

pneumonia, cardiogenic pulmonary edema, and bronchitis.

In those who present with dyspnea, the differential diagnosis includes myocardial ischemia,

pericardial effusion, pneumothorax, pulmonary embolism, pneumonia, asthma, acute

respiratory distress syndrome (ARDS), bronchiectasis, pulmonary ﬁbrosis, pleural effusion,

tuberculosis, and metabolic disturbances, acidosis and shock.

13. Which diagnostic tests are helpful in the management of COPD?

Pulse oximetry should be used in every patient with COPD. Oxygen saturation less than 90%

indicates severe hypoxia. Arterial blood gas measurements often can identify patients with

increased and continuing hypoxia, hypercarbia, and respiratory acidosis, especially if

compared with the patient’s baseline values. Check theophylline levels if indicated. Chest

radiographs are appropriate in COPD exacerbations to help manage complications and

concomitant disease. In patients with cor pulmonale, continuous cardiac monitoring may

identify any associated arrhythmias. The use of B-type natriuretic peptide (BNP) does not

substitute for clinical judgment when trying to differentiate COPD from CHF as a numeric

cut-off value that differentiates between the two diseases remains elusive. In contrast to

asthma, acute pulmonary function tests are less helpful in the emergency setting because of

the difﬁculty that sick patients with COPD have in performing these tests properly.

Differentiation of mild, moderate, and severe COPD relies on the FEV

and the ratio of FEV

forced vital capacity (FVC) ,70%. Making this calculation without formal pulmonary function

tests (PFTs) is generally not possible in the ED.

14. What are the key objectives when treating a COPD exacerbation and how are

they achieved?

The key objectives are to relieve hypoxemia, alleviate reversible bronchospasm, and treat the

underlying etiology of the exacerbation. The cornerstone of initial management is treating the

hypoxia with supplemental oxygen with a goal of oxygen saturation of 90% or greater. Despite